Tumor necrosis factor-α promotes abnormal glucose metabolism after acute pancreatitis by inducing islet β-cell apoptosis <i>via</i> Bax/Bcl-2/caspase-3 signaling pathway

TNF-α contributes to β-cell apoptosis and AGM in AP through the Bax/Bcl-2/caspase-3 signaling pathway, suggesting TNF-α as a potential therapeutic target for preventing AP-associated AGM.

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Publication Details

Journal
World Journal of Gastroenterology
Published
2025-12-19
DOI
https://doi.org/10.3748/wjg.v31.i47.113205
Citations
1
Primary Topic
Pancreatitis Pathology and Treatment
Type
article
Field-Weighted Citation Impact
2.01
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article

Tumor necrosis factor-α promotes abnormal glucose metabolism after acute pancreatitis by inducing islet β-cell apoptosis via Bax/Bcl-2/caspase-3 signaling pathway

1 citations
World Journal of Gastroenterology
Pancreatitis Pathology and Treatment
2.01
article

Tumor necrosis factor-α promotes abnormal glucose metabolism after acute pancreatitis by inducing islet β-cell apoptosis via Bax/Bcl-2/caspase-3 signaling pathway

article en
1 citations

Abstract

TNF-α contributes to β-cell apoptosis and AGM in AP through the Bax/Bcl-2/caspase-3 signaling pathway, suggesting TNF-α as a potential therapeutic target for preventing AP-associated AGM.

World Journal of GastroenterologyVol. 31(47)
Soochow University (CN), Taixing People's Hospital (CN), Taizhou First People's Hospital (CN), First Affiliated Hospital of Soochow University (CN)
Good health and well-being
Openalex Percentile: Top 10%
Pancreatitis Pathology and Treatment
2.01
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